1. Field of the Invention
The invention is generally related to medicine. In particular, the invention relates to intravascular volume and central venous pressure (CVP) measurement.
2. Background Description
Manipulation of intravascular volume (i.e., the volume of blood within blood vessels) is an important tool in the treatment of many disease states including but not limited to dehydration, congestive heart failure, renal failure, cardiogenic shock, traumatic and hemorrhagic shock, and septic shock in both their compensated and uncompensated states. However, the physical examination and medical history of a patient have not been demonstrated to produce accurate assessments of a patient's intravascular volume status. A. F. Connors, Jr., N. V Dawson, P K Shaw, H D Montenegro, A R Nara, L Martin, “Hemodynamic status in critically ill patients with and without acute heart disease,” Chest, 98(5):1200–6 (1990); N V Dawson, A F Connors, Jr., T Speroff, A Kenika, P Shaw, H R Arkes, “Hemodynamic assessment in managing the critically ill: is physician confidence warranted,” Med Decis Making, 13(3):258–66 (1993); D J Cook, “Clinical assessment of central venous pressure in the critically ill,” Am J Med Sci, 299(3):175–8 (1990); D J Cook, D L Simel, “The Rational Clinical Examination. Does this patient have abnormal central venous pressure?” Jama, 275(8):630–4 (1996); M R Shah, V Hasselblad, S S Stinnett, M Gheorghiade, K Swedberg, R M Califf, et al., “Hemodynamic profiles of advanced heart failure: Association with clinical characteristics and long-term outcomes,” J Card Fail, 7(2):105–13 (2001).
Normally, the rate of venous return to the heart equals the rate of blood pumped out of the heart and the amount of blood pumped by the right ventricle equals the amount of blood pumped by the left ventricle. A well-known relationship exists between intravascular volume and heart function based on the Frank-Starling law. A Guyton, “Heart muscle: The heart as a pump,” in A. Guyton, editor, Textbook of Medical Physiology (6th ed., Philadelphia: W. B. Saunders) (1981), pp. 150–64; A Guyton, “Cardiac output, venous return, and their regulation,” in A. Guyton (editor), Textbook of Medical Physiology, id., pp. 274–88. This principle states that within physiologic limits, the heart will pump whatever amount of blood enters the right atrium and will do so without excessive backup of blood or fluid in the veins or tissues.
When excessive central intravascular volume exists it can either be absolute from administration of consumption of excessive fluid or it can be relative secondary to failure of the pumping mechanisms of the heart from various causes. In the former case, the pumping force of the heart cannot keep up with the additional fluids. In theory, excessive fluid administration or consumption could actually result in the heart's pumping mechanisms failing through over-distension of the ventricles. In the latter case (examples of which include myocardial infarction, cardiomyopathy), fluid backs up from the left and right ventricles of the heart leading to an increase in interstitial fluid buildup in various tissues. This includes the lungs, which may result in a state of pulmonary edema leading to lung injury, hypoxemia, and potential death requiring such interventions as tracheal intubation and mechanical ventilation.
Because central or intracardiac volume plays an important role in the diagnosis and management of many chronic and acute disease states, it is helpful to have some measure of it. Conventionally, the major measure of central vascular volume has been to measure pressure either within the right atrium (or superior or inferior vena cava) or in the pulmonary artery. The former measure has been termed “central venous pressure” (CVP) and is the pressure within or very near to the right atrium. The latter measure has been termed “pulmonary artery pressure” (PAP) and when a certain device is used to occlude the forward flow in a pulmonary artery, the “pulmonary artery occlusion pressure” (PAOP). PAOP is believed to reflect the pressure within the left atrium which is in turn believed to represent the pressure within the left ventricle. It is important to understand that pressure measurements in these cases are not volume measurements, Conventionally it has been considered that these pressure measurements reflect volume within their respective areas where the measurement is being made. CVP, PAP, and PAOP have been used to assess the volume status of patients and specifically the “preload” of the heart.
“Preload” is a concept relating to the Frank-Starling law in which the volume status of the patient is adjusted (usually increased) to produce an optimal increase in cardiac output that can be induced by fluid administration alone. This fluid administration distends the contracting fibers of the heart to a length which optimizes the contractile force. It is considered optimal to follow both cardiac output and volume status simultaneously as to create cardiac output-volume/pressure curves in which CVP, PAP, or PAOP is used as a surrogate of volume. Fluid is administered until no further increase in cardiac output is noted. The CVP, PAP, or PAOP is noted and additional volume is provided to keep one or more of these pressures the same. If intravenous inotropic agents or mechanical devices are used to increase cardiac output further, the CVP, PAP, and PAOP generally falls and additional fluid administration is then warranted. Conversely, too much intravascular volume can over-distend the heart pushing the heart muscle past its optimal length for maximum contraction, which will result in a decrease in cardiac output. In these situations it is helpful to reduce preload to the heart in order to restore optimal cardiac output. This reduction in preload can take place by one or more processes including diuresis, venodilation, or afterload reduction. In each situation it is helpful to understand the magnitude of the change by measuring either CVP, PAP, or PAOP while simultaneously measuring cardiac output and/or a measurement of end-organ perfusion. In summary, it is helpful to have a measure of central intravascular volume as measured by either CVP, PAP, or PAOP.
Recently, a specially modified pulmonary artery catheter has been developed which provides a measurement of volume status and preload called “right ventricular end-diastolic volume index” (RVEDVI). A Cariou, I Laurent, JF Dhainaut, “Pulmonary artery catheterization: Modified catheters. Principles and practice of intensive care monitoring” (1998). RVEDVI is not a pressure measurement but is based on flow through the right ventricle. This measure is said to be a good indicator of preload.
Knowledge of volume status and cardiac preload is beneficial in many disease states for both diagnosis and treatment purposes. Currently, there is no non-invasive method for doing so, and the major means to measure intravascular pressure-volume is by placement of catheters into the central circulation such as the pulmonary artery catheter and its derivatives or central venous catheters. It is no simple matter to insert these catheters. Complications known to be associated with their use include infection, arrhythmia, pneumothorax, hemothorax, chylothorax, laceration of the subclavian, carotid, and femoral artery, air embolism, and retained intravenous guidewires. Thus they are not suited as screening tools and it is difficult to use them for long-term management. There is also considerable expense involved in their use along with the need for other accessories such as a fluid column as part of the pressure transduction process.
Knowledge of volume status and cardiac preload being beneficial in many disease states for both diagnosis and treatment purposes, it would be valuable if such a measure could be made less invasively than with present methods, especially noninvasively.
U.S. Pat. No. 4,566,462 (issued Jan. 28, 1986 to Janssen), for “Venous Pressure Measuring Method and Apparatus” is limited to determining venous pressure, and does not disclose determining central venous pressure. Janssen non-invasively determines blood pressure using an inflatable cuff capable of exerting pressure on a selected vein.
U.S. Pat. No. 5,447,161 (issued Sep. 5, 1995 to Blazek et al.) for “Measurement Device for Non-invasive Determination of Blood Pressure in the Veins and Arteries”, is concerned with determining blood pressure in the veins and arteries of fingers and toes. Particularly, Blazek et al. attach an air band (2) to a big toe and peripheral to the air band, apply a photoplethysmographic reflection (PPG) sensor (1) (both of which are connected to a blood pressure monitor (3)), record occlusion pressure Po in the finger band, the vein signal, and the artery signal, and raise air pressure Po in the band. When Po equals vein blood pressure Pv, the vein signal begins to rise because the blood in the veins flowing from the toe through the band is obstructed, such that the pressure in the vein can be determined. The arterial inflow into the measured area peripheral to the band is not yet impeded, so that the vein signal initially continues to rise, and the blood inflow is not impeded by the band barrier until the occlusion pressure reaches the Pd value of the pulsating arterial pressure. Blood pressure values Pv, Pd and Ps are determined by the correlation of a direct current (d.c.) signal with Po(t). Blazek et al. do not teach intravascular volume measurement, but rather, are pertinent to pressure-related situations such as early detection of thrombosis and diagnosing vein pressure behavior. Blazek et al. does not teach detection of dehydration, congestive heart failure, renal failure, cardiogenic shock, traumatic shock, hemorrhagic shock, septic shock, etc. The Blazek et al. technology is not generally applicable for determination of central intravascular pressure and volumes because their method as taught measures pressure too distal to the central circulation which would in turn overestimate central vascular pressure and hence volume.
Too-distal measurements, such as those of Blazek et al, have not conventionally been usable in determining central intravascular pressure and volumes, because overestimation would result. The overestimation would have two sources: 1) pressure in veins distal to the axillary and brachial vein will be higher and 2) as a vein is occluded (prior to collapse) venous return will begin to be impeded.
Other factors in making pressure determinations in small veins (such as the determinations of Blazek et al.) unreliable is that the these small veins are relatively sensitive to temperature, catecholamines, vasoactive peptides, gravity, edema and other factors. Thus conventional methods (such as those described by Blazek et al) that rely upon small veins are not sensitive enough to determine true intravascular pressure of a vein as that pressure relates to the pressure within the central venous compartment (right atrium, superior vena cava, inferior vena cava). As represented by Blazek in FIG. 5 the normal venous pressure in the provided example for a normal state was 18.9 mmHg. This is likely to be 3–5 times higher than the brachial-axillary pressure and hence the central venous pressure. In fact, the normal pressure in small post-capillary veins is slightly less than than half the value reported by Blazek (approximately 7 mmHg: Guyton: Textbood of Medical Physiology, 6th addition, W. B. Saunders Co: Philadelphia). This venous pressure drops further as the vein structure enlarges proximally (because veins get larger towards the central circulation and there is a pressure drop due to venous resistance from distal to more proximal venous structures).
U.S. Pat. No. 5,040,540 (issued Aug. 20, 1991 to Sackner), discloses measuring central venous pressure (CVP) based on changes in the dimensions of the neck. Sackner discloses a neck set-up and another stocking cap transducer set-up. The methods proposed by Sackner are not usable in patients over about 18 months due to the physiological basis for the CVP measurement no longer being present after cranial bones fuse in normal growth. Also, Sackner recognizes that neck volume changes detected by his transducers may be from breathing, not just from changes in blood volume, and he resorts to various methods for removing the breathing-related component, making Sackner's CVP measurements of dubious accuracy.
U.S. Pat. No. 5,904,143 (issued May 18, 1999 to Policastro et al.) discloses a non-invasive pointer-device for estimating CVP. The Policastro pointer device is not particularly accurate, and, as the inventors refer to the technology themselves, is more along the lines of an estimate.
In sum, newly available noninvasive methods (such as electrical impedance measures of intrathoracic blood volume, etc.) proposed by others cannot distinguish between intra and extravascular fluid and thus are not useable when accurate CVP measurement is needed. As a result, currently the measurement of CVP unfortunately has been limited to invasive measurements, with the current “gold standard” for measurement of central venous volume being the Swan-Ganz or pulmonary artery catheter (PAC), introduced in 1970 or the CVP catheter. While the PAC or CVP catheter can accurately measure central intravascular pressure (right atrial and right ventricular pressures, pulmonary artery pressures, and pulmonary artery occlusion or “wedge” pressure), use of this catheter constitutes an invasive technique associated with numerous complications (infections, clots, arrhthmias, etc.).
Thus, technology for monitoring CVP non-invasively while obtaining results as accurate as for invasive measurements would be a medical advance. Health benefits to patients would be seen by removing the disadvantages of invasive CVP measurement while maintaining the accuracy of such invasive measurements.